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INTRODUCTION/BACKGROUND:Antenatal lead exposure is associated with multiple adverse maternal and fetal consequences. Maternal blood lead concentrations as low as 10 µg/dL have been associated with gestational hypertension, spontaneous abortion, growth retardation, and impaired neurobehavioral development. Current treatment recommendations for pregnant women with a blood lead level (BLL) ≥ 45 µg/dL include chelation. We report a successful case of a mother with severe gestational lead poisoning treated with induction of labor in a term infant. CASE REPORT/METHODS:A 22-year-old G2P1001 female, at 38 weeks and 5 days gestation, was referred to the emergency department for an outpatient venous BLL of 53 µg/dL. The decision was made to limit ongoing prenatal lead exposure by emergent induction as opposed to chelation. Maternal BLL just prior to induction increased to 70 µg/dL. A 3510 g infant was delivered with APGAR scores of 9 and 9 at 1 and 5 min. Cord BLL at delivery returned at 41 µg/dL. The mother was instructed to avoid breastfeeding until her BLLs decreased to below 40 µg/dL, consistent with federal and local guidelines. The neonate was empirically chelated with dimercaptosuccinic acid. On postpartum day 2, maternal BLL decreased to 36 µg/dL, and the neonatal BLL was found to be 33 µg/mL. Both the mother and neonate were discharged to an alternative lead-free household on postpartum day 4.

Nitrous oxide is a commonly used inhaled anesthetic for medical procedures, as well as a drug of abuse throughout the world. Excessive nitrous oxide inhalation has been shown to cause a functional vitamin B12 deficiency and hyperhomocysteinemia, which can lead to peripheral neuropathy and hypercoagulability, respectively. While the development of neurologic toxicity from chronic nitrous oxide abuse (i.e., encephalopathy, myelopathy, and neuropathy) has been previously described, the thrombotic potential of chronic nitrous oxide abuse is less known. The authors report two cases of nitrous oxide abuse leading to both neurologic and thrombotic complications.
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DISCLAIMER/CONCLUSIONS:In an effort to expedite the publication of articles, AJHP is posting manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. PURPOSE/OBJECTIVE:The case of a patient with a massive acute enoxaparin overdose managed with observation and minimal doses of protamine sulfate is reported. SUMMARY/CONCLUSIONS:Acute enoxaparin overdoses are uncommonly reported and management is widely variable. A 25-year-old man presented to the emergency department (ED) shortly after reporting that he had attempted suicide by injecting himself with 31 syringes of 80 mg of enoxaparin (a total of 2,480 mg) in the abdomen and other areas of his body. The patient also had self-inflicted superficial lacerations of the forearm. Due to concern over suspected compartment syndrome in the forearm, 25 mg of protamine was administered. Approximately 11 hours after reported enoxaparin self-injection, the patient's activated partial thromboplastin time (aPTT) was 206 seconds, prompting administration of an additional 50 mg of protamine. Three hours later, the aPTT had decreased to 79 seconds, then rose over several hours to 127 seconds before gradually declining to normal values. Protamine administration had no appreciable impact on anti-factor Xa activity. The patient did not require any blood products during the hospital admission. There were no further complications, and the patient was discharged to the inpatient psychiatry service on hospital day 8. CONCLUSION/CONCLUSIONS:The case highlights the role of protamine as a reversal agent in the management of low-molecular-weight heparin overdoses. The optimal dosing and efficacy of protamine for this indication needs further investigation.

Fluoroquinolones are commonly used antimicrobials with multiple known adverse effects, yet overdose events are rarely reported. Here, we report a case of a previously healthy middle-aged woman who unintentionally ingested 7 g of levofloxacin in one dose. Thereafter, she presented to the emergency department with hemiparesis concerning for ischaemic stroke and was administered tissue plasminogen activator. Her brain imaging showed no ischaemic injury and her symptoms resolved within 24 hours; this is consistent with a transient ischaemic attack. Our case highlights potential adverse effects of an acute overdose of levofloxacin that has not previously been well described.